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Questions and Answers
Which of the following statements about the use of uricosuric agents like probenecid and sulfinpyrazone is correct?
Which of the following statements about the use of uricosuric agents like probenecid and sulfinpyrazone is correct?
- They should not be used during an acute gout attack as they may precipitate an attack. (correct)
- They do not interact with other drugs that are actively secreted by the renal tubules.
- Aspirin and other salicylates can be used concomitantly to enhance the uricosuric effect.
- They can be used alone for the treatment of chronic gout without the need for colchicine.
What is the primary side effect associated with the use of uricosuric agents like probenecid and sulfinpyrazone?
What is the primary side effect associated with the use of uricosuric agents like probenecid and sulfinpyrazone?
- Urolithiasis (formation of urate stones) (correct)
- Hepatotoxicity
- Nephrotoxicity
- Cardiovascular events
How do probenecid and allopurinol interact?
How do probenecid and allopurinol interact?
- Probenecid and allopurinol have no clinically significant interactions.
- Probenecid increases the half-life of allopurinol and enhances its uricosuric effect.
- Allopurinol increases the clearance of probenecid, thereby reducing its uricosuric effect.
- Probenecid decreases the clearance of allopurinol, thereby increasing dose requirements of allopurinol. (correct)
Which of the following drugs should not be used concomitantly with uricosuric agents like probenecid and sulfinpyrazone?
Which of the following drugs should not be used concomitantly with uricosuric agents like probenecid and sulfinpyrazone?
What is the potential role of interleukin-1 (IL-1) inhibitors in the treatment of gout?
What is the potential role of interleukin-1 (IL-1) inhibitors in the treatment of gout?
What is the typical presentation of acute gout?
What is the typical presentation of acute gout?
Which of the following drugs is not recommended for acute gout treatment?
Which of the following drugs is not recommended for acute gout treatment?
What is the action of Colchicine when used for gout prophylaxis?
What is the action of Colchicine when used for gout prophylaxis?
Which of the following is an unlabeled use of Colchicine?
Which of the following is an unlabeled use of Colchicine?
In what form should Colchicine be taken for gout prophylaxis?
In what form should Colchicine be taken for gout prophylaxis?
Which of the following drugs is contraindicated in patients with glucose-6-phosphate dehydrogenase deficiency?
Which of the following drugs is contraindicated in patients with glucose-6-phosphate dehydrogenase deficiency?
Which of the following is a potential side effect of pegloticase?
Which of the following is a potential side effect of pegloticase?
What is the mechanism of action of probenecid and sulfinpyrazone?
What is the mechanism of action of probenecid and sulfinpyrazone?
Which of the following is a concern associated with the development of antibodies against pegloticase?
Which of the following is a concern associated with the development of antibodies against pegloticase?
Which of the following statements is true regarding the monitoring of pegloticase therapy?
Which of the following statements is true regarding the monitoring of pegloticase therapy?
What is the main risk associated with co-administration of NSAIDs with anticoagulants like warfarin?
What is the main risk associated with co-administration of NSAIDs with anticoagulants like warfarin?
What effect does the co-administration of NSAIDs have on the nephrotoxicity of cyclosporine and tacrolimus?
What effect does the co-administration of NSAIDs have on the nephrotoxicity of cyclosporine and tacrolimus?
Why were most coxibs either severely restricted in use or withdrawn from the market?
Why were most coxibs either severely restricted in use or withdrawn from the market?
How do quinolone antimicrobials interact with NSAIDs when co-administered?
How do quinolone antimicrobials interact with NSAIDs when co-administered?
What is the primary reason for the lower rate of ulceration associated with COX-2 inhibitors compared to older NSAIDs?
What is the primary reason for the lower rate of ulceration associated with COX-2 inhibitors compared to older NSAIDs?
Which NSAID is most likely to be recommended for a patient with a history of gastrointestinal bleeding?
Which NSAID is most likely to be recommended for a patient with a history of gastrointestinal bleeding?
Which NSAID has the least potential for inhibiting COX-1, and therefore causing gastrointestinal side effects?
Which NSAID has the least potential for inhibiting COX-1, and therefore causing gastrointestinal side effects?
Which NSAID is most likely to undergo enterohepatic circulation, leading to side effects in the lower intestine?
Which NSAID is most likely to undergo enterohepatic circulation, leading to side effects in the lower intestine?
Which NSAID is a ketone prodrug that is metabolized to the active acidic form?
Which NSAID is a ketone prodrug that is metabolized to the active acidic form?
Which NSAID is most likely to have less gastric irritation compared to other NSAIDs?
Which NSAID is most likely to have less gastric irritation compared to other NSAIDs?
Which class of drugs includes Aspirin, Na-salicylate, and diflunisal?
Which class of drugs includes Aspirin, Na-salicylate, and diflunisal?
Which of the following NSAIDs belongs to the Oxicams class?
Which of the following NSAIDs belongs to the Oxicams class?
Which drug is a Pyrrolo-pyrrole NSAID?
Which drug is a Pyrrolo-pyrrole NSAID?
Which NSAID has both peripheral and central antipyretic effects?
Which NSAID has both peripheral and central antipyretic effects?
Which class of NSAIDs includes Ibuprofen, Naproxen, and fenoprofen?
Which class of NSAIDs includes Ibuprofen, Naproxen, and fenoprofen?
How does aspirin achieve its anti-inflammatory effect?
How does aspirin achieve its anti-inflammatory effect?
What is the primary mechanism through which aspirin prevents myocardial infarction?
What is the primary mechanism through which aspirin prevents myocardial infarction?
Why is the inhibition of COX enzymes by aspirin significant in its mechanism of action?
Why is the inhibition of COX enzymes by aspirin significant in its mechanism of action?
Which effect of aspirin occurs at high doses?
Which effect of aspirin occurs at high doses?
How does aspirin differ from other NSAIDs in terms of COX enzyme inhibition?
How does aspirin differ from other NSAIDs in terms of COX enzyme inhibition?
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